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Articles by E. E Moore
Total Records ( 4 ) for E. E Moore
  C. C Cothren , W. L Biffl , E. E Moore , J. L Kashuk and J. L. Johnson

Hypothesis  We hypothesize that the 2 antithrombotic treatment regimens, systemic heparin sodium vs antiplatelet agents, are equivalent for the treatment of blunt cerebrovascular injuries (BCVIs) to prevent devastating injury-related strokes.

Design  Retrospective review of a prospective database.

Setting  Level I trauma center.

Patients  Patients with BCVIs from January 1, 1997, to January 1, 2007.

Main Outcome Measures  Incidence of cerebrovascular accident (CVA), stratified by treatment.

Results  During the study period, 422 BCVIs were identified in 301 patients (64.8% men; mean [SEM] age, 37.0 [0.8] years; mean [SEM] injury severity score, 27.0 [0.9]). A total of 22 patients presented with neurologic ischemia, and 5 patients sustained CVAs after embolization and/or stenting of an injury. Treatment was initiated for 282 asymptomatic BCVIs (heparin, 192; aspirin, 67; aspirin and/or clopidogrel, 23); 1 patient had a CVA (0.5%). Of 107 patients with untreated, asymptomatic BCVIs, 23 (21.5%) had a CVA. For untreated patients sustaining BCVI-related CVAs, the mean (SEM) time to diagnosis was 58 (10) hours. For those who did not exhibit symptoms within 2 hours of injury, mean time to diagnosis of CVA was 75 (11) hours. Injury healing rates (heparin, 39%; aspirin, 43%; aspirin/clopidogrel, 46%) and injury progression rates (12%; 10%; 15%) were equivalent between therapeutic regimens.

Conclusions  With an overall CVA risk of 21% and a documented latent period, comprehensive screening, early diagnosis, and institution of antithrombotic therapy for BCVI are clearly warranted. The type of treatment, heparin vs antiplatelet agents, does not appear to affect either stroke risk or injury healing rates.

  J. L Johnson , E. E Moore , J. L Kashuk , A Banerjee , C. C Cothren , W. L Biffl and A. Sauaia

Hypothesis  Transfusion of fresh frozen plasma (FFP) and platelets is independently associated with the development of multiple organ failure (MOF) in critically injured patients.

Design  Prospective cohort study.

Setting  Academic regional level I trauma center.

Patients  From 1992 to 2004, a total of 1440 critically injured patients were admitted to our surgical intensive care unit and survived at least 48 hours. Of these, 1415 had complete data on age, Injury Severity Score (ISS), and units of FFP, platelets, and packed red blood cells (PRBCs) transfused. Multiple organ failure was defined using the Denver MOF score. Multiple logistic regression analysis was used to adjust transfusion of FFP, platelets, and PRBCs for known MOF risk factors.

Main Outcome Measure  Multiple organ failure.

Results  The mean (SD) ISS was 29.3 (11.3), and the mean (SD) patient age was 37.4 (16.6) years. Among 1440 patients, 346 (24.0%) developed MOF, and 118 (8.2%) died. Multiple logistic regression analysis detected a significant interaction between units of FFP and PRBCs transfused (P < .001). Regardless of the units of PRBCs transfused, FFP transfusion was independently associated with the development of MOF. However, the deleterious effect associated with FFP transfusion was more prominent among patients receiving fewer than 6 U of PRBCs. Platelet transfusion was unassociated with MOF after adjustment for age, ISS, and FFP and PRBC transfusion.

Conclusions  Early transfusion of FFP is associated with an increased risk of postinjury MOF, even after adjusting for age, ISS, and PRBC transfusion. Caution is warranted in developing protocols for empirical FFP transfusion. Specifically, transfusion triggers for FFP should be reexamined, as well as the practice of delivering FFP in fixed ratios to the units of PRBCs transfused.

  A. J Luk , G. P Levin , E. E Moore , X. H Zhou , B. R Kestenbaum and H. K. Choi

Objectives. While studies have suggested that gout and hyperuricaemia are associated with the risk of premature death, none has investigated the role of urate-lowering therapy on this critical outcome. We examined the impact of allopurinol, the most commonly used urate-lowering drug, on the risk of mortality in hyperuricaemic patients.

Methods. From a population of hyperuricaemic veterans of [serum urate level >416 µmol/l (7.0 mg/dl)] at least 40 years of age, we compared the risk of death between incident allopurinol users (n = 2483) and non-users (n = 7441). We estimated the multivariate mortality hazard ratio (HR) of allopurinol use with Cox proportional hazards models.

Results. Of the 9924 veterans (males, 98% and mean age 62.7 years), 1021 died during the follow-up. Patients who began treatment with allopurinol had worse prognostic factors for mortality, including higher BMI and comorbidities. After adjusting for baseline urate levels, allopurinol treatment was associated with a lower risk of all-cause mortality (HR 0.78; 95% CI 0.67, 0.91). Further adjustment with other prognostic factors did not appreciably alter this estimate (HR 0.77; 95% CI 0.65, 0.91). The mean change from baseline in serum urate within the allopurinol group was –111 µmol/l (–1.86 mg/dl). Adjusting for baseline urate level, allopurinol users had a 40 µmol/l (0.68 mg/dl) lower follow-up serum urate value than controls (95% CI –0.55, –0.81).

Conclusion. Our findings indicate that allopurinol treatment may provide a survival benefit among patients with hyperuricaemia.

  P. C Eckels , A Banerjee , E. E Moore , N. J. D McLaughlin , L. M Gries , M. R Kelher , K. M England , F Gamboni Robertson , S. Y Khan and C. C. Silliman

Receptor signaling is integral for adhesion, emigration, phagocytosis, and reactive oxygen species production in polymorphonuclear neutrophils (PMNs). Priming is an important part of PMN emigration, but it can also lead to PMN-mediated organ injury in the host. Platelet-activating factor (PAF) primes PMNs through activation of a specific G protein-coupled receptor. We hypothesize that PAF priming of PMNs requires clathrin-mediated endocytosis (CME) of the PAF receptor (PAFr), and, therefore, amantadine, known to inhibit CME, significantly antagonizes PAF signaling. PMNs were isolated by standard techniques to >98% purity and tested for viability. Amantadine (1 mM) significantly inhibited the PAF-mediated changes in the cellular distribution of clathrin and the physical colocalization [fluorescence resonance energy transfer positive (FRET+)] of early endosome antigen-1 and Rab5a, known components of CME and similar to hypertonic saline, a known inhibitor of CME. Furthermore, amantadine had no effect on the PAF-induced cytosolic calcium flux; however, phosphorylation of p38 MAPK was significantly decreased. Amantadine inhibited PAF-mediated changes in PMN physiology, including priming of the NADPH oxidase and shape change with lesser inhibition of increases in CD11b surface expression and elastase release. Furthermore, rimantadine, an amantadine analog, was a more potent inhibitor of PAF priming of the N-formyl-methionyl-leucyl-phenylalanine-activated oxidase. PAF priming of PMNs requires clathrin-mediated endocytosis that is inhibited when PMNs are pretreated with either amantadine or rimantadine. Thus, amantadine and rimantadine have the potential to ameliorate PMN-mediated tissue damage in humans.

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